ArticleCellular signalling2020
TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages through JNK signaling pathway.
Article in Cellular signalling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Potential Therapeutic Roles of Icariin in Inflammatory Diseases: From Molecular Mechanisms to Clinical Translation Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- TRIM65 accelerates VSMC-derived foam cell formation and arteriosclerosis progression by inhibiting mitophagy.Molecular and cellular biochemistry · 2026Article
- Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions.Frontiers in immunology · 2026Review
- Emerging Role of Calycosin in Inflammatory Diseases: Molecular Mechanisms and Potential Therapeutic Applications.Biomolecules · 2025Review
- Effect of TRIM67 knockout on inflammation and macrophage survival in Salmonella Typhimurium-infected mice.Archives of microbiology · 2025Article
- Okra polysaccharide mitigates carrageenan-induced thrombosis in mice by regulating inflammation and oxidative stress.Frontiers in pharmacology · 2025Article
- The Nrf Family and Its Cardioprotective Potential: Mechanisms, Functions, and Therapeutic Perspectives.Drug design, development and therapy · 2025Review
- TRIM59 is required for mouse GC-1 cell maintenance through modulating the ubiquitination of AXIN1.Heliyon · 2024Article
- The Role of Tripartite Motif Family Proteins in Chronic Liver Diseases: Molecular Mechanisms and Therapeutic Potential.Biomolecules · 2024Review
- Myeloid CellJournal of inflammation research · 2024Article
- NRF1 knockdown alleviates lipopolysaccharide-induced pulmonary inflammatory injury by upregulating DKK3 and inhibiting the GSK-3β/β-catenin pathway.Clinical and experimental immunology · 2023Article
- Identification of KeyInternational journal of molecular sciences · 2023Article
- GRaNIE and GRaNPA: inference and evaluation of enhancer-mediated gene regulatory networks.Molecular systems biology · 2023Article
- Osteopontin Promotes Macrophage M1 Polarization by Activation of the JAK1/STAT1/HMGB1 Signaling Pathway in Nonalcoholic Fatty Liver Disease.Journal of clinical and translational hepatology · 2023Article
- LPS inhibits TRIM65 expression in macrophages and C57BL/6J mouse by activating the ERK1/2 signaling pathway.Experimental and therapeutic medicine · 2023Article
- TRIM59 attenuates ox-LDL-induced endothelial cell inflammation, apoptosis, and monocyte adhesion through AnxA2.Annals of translational medicine · 2023Article
- Article
- Role of Sp1 in atherosclerosis.Molecular biology reports · 2022Review
- SP1 Promotes HDAC4 Expression and Inhibits HMGB1 Expression to Reduce Intestinal Barrier Dysfunction, Oxidative Stress, and Inflammatory Response after Sepsis.Journal of innate immunity · 2022Article
- METTL3-Mediated N6-Methyladenosine Modification of Trim59 mRNA Protects Against Sepsis-Induced Acute Respiratory Distress Syndrome.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Activated macrophages play an important role in many inflammatory diseases including septic shock and atherosclerosis. TRIM59 has been showed to participate in many pathological processes, such as inflammation, cytotoxicity and tumorigenesis. However, the molecular mechanisms controlling its expression in activated macrophages are not fully understood. Here we report that TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages. TRIM59 is highly expressed in macrophages, and markedly decreased by LPS stimuli in vivo and in vitro. TRIM59 promoter activity is also significantly suppressed by LPS and further analysis demonstrated that Sp1 and Nrf1 directly bound to the proximal promoter of TRIM59 gene. LPS treatment significantly decreased Sp1 expression, nuclear translocation and reduced its binding to the promoter, whereas increased Nrf1 expression, nuclear translocation and enhanced its binding to the promoter. Moreover, LPS-decreased TRIM59 expression was reversed by JNK inhibitor. Finally, TRIM59 level is significantly decreased during atherosclerosis progression. Taken together, our results demonstrated that TRIM59 expression was precisely regulated by Sp1 and Nrf1 in LPS-activated macrophages, which may be dependent on the activation of JNK signaling pathway and TRIM59 may be a potential therapeutic target for inflammatory diseases such as atherosclerosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.